Morris, Norman

Introduction/Aim: Heart failure (HF) is a complex clinical syndrome, characterised by reduced exercise capacity (VO 2 peak) and quality of life leading to premature death. The reduction in VO 2 peak is a key prognostic indicator, and improving exercise capacity remains a critical therapeutic target. In athletes, the use of intermittent hypoxia training to improve VO 2 peak and performance is well established. Changes in VO 2 peak are typically accompanied by improved oxygen carrying capacity with increased haemoglobin (Hb) concentration mediated through increased erythropoietin (EPO) production in the kidney. The purpose of this pilot study was to examine the feasibility of using intermittent hypoxia training in individuals with HF, and examine changes in VO 2 peak, EPO and Hb. We hypothesised that intermittent hypoxia training would be feasible, well tolerated, and improve VO 2 peak, EPO production, Hb concentration in HF with reduced ejection fraction (HFrEF). Methods: Ten male participants with stable, optimally managed HFrEF (Age: 73 ± 5 yr; Ejection Fraction: 37 ± 11%) participated in the study. The training stimulus consisted of 12 x 60-minute sessions of intermittent hypoxia over a 2-week period. During each 60-minute session participants received 6 x 5 minutes of pulsed, reduced FIO 2 exposures interspersed with 5 min of normoxia (total of 30 min hypoxic exposure per session). All participants commenced at 18% FIO 2 , which was decreased to 12% by the 3-4th sesion, as tolerated. Throughout each exposure, oxygen saturation (SpO 2 ), heart rate, blood pressure and dyspnoea (modified Borg scale) were monitored every 5 min. Changes in VO 2 peak were measured using a cycle ergometry, cardiopulmonary exercise test. Changes in VO 2 peak, N-terminal pro B-type natriuretic peptide (NT-proBNP), EPO and Hb concentration were measured pre and immediately post intermittent hypoxic training. Results: All participants completed between 10-12 (median n=12) sessions over the 2-week period. Intermittent hypoxia was well-tolerated with no adverse events. The mean SpO 2 during the hypoxic exposure was 88 ± 4%, and median reported dyspnoea 0 (range 0-1). Following 2 weeks of intermittent hypoxic training, there were significant increases in VO 2 peak (mean difference[MD]: +1.18 mL·kg - ¹·min - ¹, 95% CI 0.47 to 1.89, p = 0.010); EPO (MD: +3.33 IU/L, 95% CI 1.35 to 5.32, p = 0.011); with a modest increase in Hb concentration that approached significance (MD: +4.00 g/L, 95% CI 0.51 to 7.49, p = 0.055). NT-proBNP remained unchanged (MD: –107 pg/mL, 95% CI –356 to 142, p = 0.424). Conclusion The results of this pilot study suggest that in clinically stable HFrEF, 2 weeks of intermittent hypoxic training results in a significant improvement in VO 2 peak, accompanied by increases in EPO and potentially levels of Hb. In our participants, this 60-minute pulsed intermittent hypoxic protocol was extremely well tolerated without any adverse effects, and may improve oxygen carrying capacity of the blood in HFrEF. Further research on the mechanisms of adaptation and the translation of the response into different HF phenotypes is warranted. Supported By: The Prince Charles Hospital Foundation Innovation Grant INN202-049 and Griffith University. This abstract was presented at the American Physiology Summit 2026 and is only available in HTML format. There is no downloadable file or PDF version. The Physiology editorial board was not involved in the peer review process.

Purpose: Literature on early mobilization and exercise training in patients recovering from acute heart failure (AHF) is promising. However, there lacks uniformity in the time of initiation, exercise prescription, safety criteria, and termination criteria. Thus, the aim was to develop a mobilization algorithm for patients recovering from AHF. Methods: A modified web-based Delphi process was undertaken involving 15 panelists from across the globe. In Round 1, new variables, modifications to suggested variables, and agreement-disagreement within the panelists were obtained. In Round 2, agreement on a 5-point Likert scale was obtained. In Round 3, the algorithm was compiled, and excluded statements were discussed via web-based calls. The new variables were grouped into themes via an inductive process. The level of agreement and rating for each statement were analyzed using descriptive statistics, including frequency and percentages. We used Kappa statistics to examine the level of agreement between the panelists for each criterion. The consensus criterion was defined a priori as statements with a mean rating of ≥4 on the 5-point Likert scale by ≥70% of the panelists and Kendall’s coefficient of concordance ( W ) of ≥0.3 between panelists. Results: From Round 1, 54 new variables were obtained. More than two-thirds (118/170, 69%) of statements reached consensus and reported a fair level of agreement between panelists ( W ≥ 0.3). The final algorithm with all its criteria received a 100% (13/13) consensus. Conclusion: Physician-referral criteria, physiotherapy assessment process, exercise prescription, safety criteria, and termination criteria were formulated for early mobilization and exercise training for patients recovering from AHF.

High-intensity endurance exercise elicits acute cardiac imbalances that may be an important stimulus for adaptive cardiac remodeling. This study highlights that following a bout of high-intensity exercise that is typical of routine day-to-day cycling training, exercise-induced autonomic, biochemical, and functional cardiac imbalances are attenuated in middle-aged relative to young well-trained cyclists. These findings suggest that aging may alter exercise-induced stress stimulus response that initiates cardiac remodeling in Athlete’s Heart.

We propose that abnormalities of the pulmonary system contribute significantly to the exertional dyspnea and exercise intolerance observed in patients with chronic heart failure. Interventions designed to address the deleterious pulmonary manifestations of heart failure may, therefore, yield promising improvements in exercise tolerance in this population.

Heart failure (HF) patients are susceptible to heat strain during exercise, secondary to blunted skin blood flow (SkBF) responses, which may be explained by impaired nitric oxide (NO)-dependent vasodilation. Folic acid improves vascular endothelial function and SkBF through NO-dependent mechanisms in healthy older individuals and patients with cardiovascular disease. We examined the effect of folic acid supplementation (5 mg/day for 6 wk) on vascular function [brachial artery flow-mediated dilation (FMD)] and SkBF responses [cutaneous vascular conductance (CVC)] during 60 min of exercise at a fixed metabolic heat production (300 ẆHprod) in a 30°C environment in 10 patients with HF (New York Heart Association Class I–II) and 10 healthy controls (CON). Serum folic acid concentration increased in HF [preintervention (pre): 1.4 ± 0.2; postintervention (post): 8.9 ± 6.7 ng/ml, P = 0.01] and CON (pre: 1.3 ± 0.6; post: 5.2 ± 4.9 ng/ml, P = 0.03). FMD improved by 2.1 ± 1.3% in HF ( P < 0.01), but no change was observed in CON postintervention ( P = 0.20). During exercise, the external workload performed on the cycle ergometer to attain the fixed level of heat production for exercise was similar between groups (HF: 60 ± 13; CON: 65 ± 20 external workload, P = 0.52). Increases in CVC during exercise were similar in HF (pre: 0.89 ± 0.43; post: 0.83 ± 0.45 au/mmHg, P = 0.80) and CON (pre: 2.01 ± 0.79; post: 2.03 ± 0.72 au/mmHg, P = 0.73), although the values were consistently lower in HF for both pre- and postintervention measurement intervals ( P < 0.05). These findings demonstrate that folic acid improves vascular endothelial function in patients with HF but does not enhance SkBF during exercise at a fixed metabolic heat production in a warm environment.

Chest wall strapping has been used to assess mechanisms of dyspnea with restrictive lung disease. This study examined the hypothesis that dyspnea with restriction depends principally on the degree of reflex ventilatory stimulation. We compared dyspnea at the same (iso)ventilation when added dead space provided a component of the ventilatory stimulus during exercise. Eleven healthy men undertook a randomized controlled crossover trial that compared four constant work exercise conditions: 1) control (CTRL): unrestricted breathing at 90% gas exchange threshold (GET); 2) CTRL+dead space (DS): unrestricted breathing with 0.6-l dead space, at isoventilation to CTRL due to reduced exercise intensity; 3) CWS: chest wall strapping at 90% GET; and 4) CWS+DS: chest strapping with 0.6-l dead space, at isoventilation to CWS with reduced exercise intensity. Chest strapping reduced forced vital capacity by 30.4 ± 2.2% (mean ± SE). Dyspnea at isoventilation was unchanged with CTRL+DS compared with CTRL (1.93 ± 0.49 and 2.17 ± 0.43, 0–10 numeric rating scale, respectively; P = 0.244). Dyspnea was lower with CWS+DS compared with CWS (3.40 ± 0.52 and 4.51 ± 0.53, respectively; P = 0.003). Perceived leg fatigue was reduced with CTRL+DS compared with CTRL (2.36 ± 0.48 and 2.86 ± 0.59, respectively; P = 0.049) and lower with CWS+DS compared with CWS (1.86 ± 0.30 and 4.00 ± 0.79, respectively; P = 0.006). With unrestricted breathing, dead space did not change dyspnea at isoventilation, suggesting that dyspnea does not depend on the mode of reflex ventilatory stimulation in healthy individuals. With chest strapping, dead space presented a less potent stimulus to dyspnea, raising the possibility that leg muscle work contributes to dyspnea perception independent of the ventilatory stimulus. NEW & NOTEWORTHY Chest wall strapping was applied to healthy humans to simulate restrictive lung disease. With chest wall strapping, dyspnea was reduced when dead space substituted for part of a constant exercise stimulus to ventilation. Dyspnea associated with chest wall strapping depended on the contribution of leg muscle work to ventilatory stimulation. Chest wall strapping might not be a clinically relevant model to determine whether an alternative reflex ventilatory stimulus mimics the intensity of exertional dyspnea.

AbstractHeart failure (HF) patients appear to exhibit impaired thermoregulatory capacity during passive heating, as evidenced by diminished vascular conductance. Although some preliminary studies have described the thermoregulatory response to passive heating inHF, responses during exercise in the heat remain to be described. Therefore, the aim of this study was to compare thermoregulatory responses inHFand controls (CON) during exercise in the heat. TenHF(NYHAclasses I–II) and eightCONwere included. Core temperature (Tc), skin temperature (Tsk), and cutaneous vascular conductance (CVC) were assessed at rest and during 1 h of exercise at 60% of maximal oxygen uptake. Metabolic heat production (Hprod) and the evaporative requirements for heat balance (Ereq) were also calculated. Whole‐body sweat rate was determined from pre–post nude body mass corrected for fluid intake. WhileHprod(HF: 3.9 ± 0.9;CON: 6.4 ± 1.5 W/kg) andEreq(HF: 3.3 ± 0.9;CON: 5.6 ± 1.4 W/kg) were lower (P < 0.01) forHFcompared toCON, both groups demonstrated a similar rise inTc(HF: 0.9 ± 0.4;CON: 1.0 ± 0.3°C). Despite this similar rise inTc,Tsk(HF: 1.6 ± 0.7;CON: 2.7 ± 1.2°C), and the elevation inCVC(HF: 1.4 ± 1.0;CON: 3.0 ± 1.2 au/mmHg) was lower (P < 0.05) inHFcompared toCON. Additionally, whole‐body sweat rate (HF: 0.36 ± 0.15;CON: 0.81 ± 0.39 L/h) was lower (P = 0.02) inHFcompared toCON. Patients withHFappear to be limited in their ability to manage a thermal load and distribute heat content to the body surface (i.e., skin), secondary to impaired circulation to the periphery.